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Caisson disease [decompression sickness]
ICD-10 T703
ICD-9 993.3
OMIM [1]
DiseasesDB 3491
MedlinePlus [2]
eMedicine emerg/121
MeSH C21.866.120.248

Decompression sickness (DCS), the diver’s disease, the bends, caisson disease is a decompression effect, the name given to a variety of symptoms suffered by a person exposed to a decrease (nearly always after a big increase) in the pressure around the body.[1] The body must adapt to the pressure following a rapid ascent. It is a type of diving hazard and dysbarism.


Decompression sickness can happen in these situations:

File:Preparing for recompression.jpg

These situations cause excess inert gases, which have dissolved in body liquids and tissues while the gas was being inhaled at higher pressure, to come out of physical solution as the pressure reduces and form gas bubbles within the body. The main inert gas for those who breathe air is nitrogen. The bubbles result in the symptoms of decompression sickness.[1][2][10]

According to Henry's Law, when the pressure of a gas over a liquid is decreased, the amount of gas dissolved in that liquid will also decrease. A good practical demonstration of this law is offered by opening a soft drink can or bottle. During the manufacture of the drink, carbon dioxide gas at higher than atmospheric pressure is sealed in the container with the liquid. Some of the gas goes into solution with the liquid due to the higher pressure. When the container is opened, the free gas can be heard escaping from the container and bubbles form in the liquid. These bubbles are the previously dissolved carbon dioxide gas coming out of solution as a result of the reduction to atmospheric pressure of the gas inside the container.

Similarly, inert gases are normally stored throughout the body, such as within tissues and liquids, in physical solution. When the body is exposed to decreased pressures, such as when flying an un-pressurized aircraft to altitude or during a scuba ascent through water, the excess inert gas comes out of solution in a process called "outgassing" or "offgassing". Normally most offgassing occurs by gas exchange at the lungs during exhalation[2][11][12]. If inert gas is forced to come out of solution too quickly, bubbles form inside the body and are unable to leave through the lungs causing the signs and symptoms of the "bends" which can be itching skin and rashes, joint pain, sensory system failure, paralysis, and death.[2][13]

An air embolism, caused by other processes, can have many of the same symptoms as DCS. The two conditions are grouped together under the name decompression illness or DCI.[2][13]


  • 1670: Boyle demonstrated that a reduction in ambient pressure could lead to bubble formation in living tissue. This description of a viper in a vacuum was the first recorded description of decompression sickness.
  • 1769: Giovanni Morgagni described the post mortem findings of air in cerebral circulation and surmised this was the cause of death.
  • 1841: First documented case of decompression sickness, reported by a mining engineer who observed pain and muscle cramps among coal miners working in mine shafts air-pressurized to keep water out.
  • 1870: Bauer published outcomes of 25 paralyzed caisson workers.

From 1870 to 1910 all prominent features were established. Explanations at the time included: cold or exhaustion causing reflex spinal cord damage; electricity cause by friction on compression; or organ congestion and vascular stasis caused by decompression.

  • 1871: The St Louis Eads Bridge employed 352 compressed air workers including Dr. Alphonse Jaminet as the physician in charge. There were 30 seriously injured and 12 fatalities. Dr. Jaminet developed decompression sickness and his personal description was the first such recorded.
  • 1872: The similarity between decompression sickness and iatrogenic air embolism as well as the relationship between inadequate decompression and decompression sickness was noted by Friedburg. He suggested that intravascular gas was released by rapid decompression and recommended: slow compression and decompression; four hour working shifts; limit to maximum depth 44.1 psig (4 ATA); using only healthy workers; and recompression treatment for severe cases.
  • 1873: Dr. Andrew Smith first utilized the term "caisson disease" describing 110 cases of decompression sickness as the physician in charge during construction of the Brooklyn Bridge. The project employed 600 compressed air workers. Recompression treatment was not used. The project chief engineer Washington Roebling suffered from caisson disease. (He took charge after his father John Augustus Roebling died of tetanus.) Washington's wife, Emily, helped manage the construction of the bridge after his sickness confined him to his home in Brooklyn. He battled the after-effects of the disease for the rest of his life. During this project, decompression sickness became known as "The [Grecian] Bends" because afflicted individuals characteristically arched their backs: this is possibly reminiscent of a then fashionable women's dance maneuver known as the Grecian Bend or as historian David McCullough asserts in The Great Bridge it was a crude reference to "Greek" or anal sex.[14]
  • 1900: Leonard Hill used a frog model to prove that decompression causes bubbles and that recompression resolves them.
  • 1908: "The Prevention of Compressed Air Illness" was published by J. S. Haldane, Boycott and Damant recommending staged decompression.[15] These tables were accepted for use by the Royal Navy.[16]

Predisposing factorsEdit


  • Magnitude of the pressure reduction[6][17][7]: A large pressure reduction is more likely to cause DCS than a small one. For example, the ambient pressure halves by ascending during a dive from 10 metres (Template:Convert/ft)Template:Convert/test/A (2 bar) to the surface (1 bar), or by flying from sea level (1 bar) to an altitude of 5,000 metres (Template:Convert/ft)Template:Convert/test/A (0.5 bar) in an un-pressurized aircraft. Diving and then flying shortly afterwards increases the pressure reduction as does diving at high altitude.
  • Repetitive exposures: Repetitive dives or ascents to altitudes above 5,500 metres (Template:Convert/ft)Template:Convert/test/A within a short period of time (a few hours) also increase the risk of developing altitude DCS.[6][17]
  • Rate of ascent: The faster the ascent, the greater the risk of developing altitude DCS. An individual exposed to a rapid decompression (high rate of ascent) above 5,500 metres (Template:Convert/ft)Template:Convert/test/A has a greater risk of altitude DCS than being exposed to the same altitude but at a lower rate of ascent.[6][17]
  • Time at altitude: The longer the duration of the flight to altitudes of 5,500 metres (Template:Convert/ft)Template:Convert/test/A and above, the greater the risk of altitude DCS.[6]


  • Age: There are some reports indicating a higher risk of altitude DCS with increasing age.[1][17]
  • Previous injury: There is some indication that recent joint or limb injuries may predispose individuals to developing decompression related bubbles.[1][18]
  • Ambient temperature: There is some evidence suggesting that individual exposure to very cold ambient temperatures may increase the risk of altitude DCS.[1][17] Decompression sickness risk can be reduced by increased ambient temperature during decompression following dives in cold water.[19]
  • Body Type: Typically, a person who has a high body fat content is at greater risk of DCS.[1][17][20] Due to poor blood supply, nitrogen is stored in greater amounts in fat tissues. Although fat represents only 15 percent of a normal adult body, it stores over half of the total amount of nitrogen (about 1 litre) normally dissolved in the body.
  • Alcohol consumption/dehydration: While conventional wisdom would have one believe that the after effects of alcohol consumption increase the susceptibility to DCS through increased dehydration[17], one study concluded that alcohol consumption did not increase the risk of DCS.[21]. Studies by Walder concluded that decompression sickness could be reduced in aviators when the serum surface tension was raised by drinking isotonic saline[17][22]. The high surface tension of water is generally regarded as helpful in controlling bubble size, hence avoiding dehydration is recommended by most experts.
  • Patent foramen ovale: A hole between the atrial chambers of the heart in the fetus is normally closed by a flap with the first breaths at birth. In up to 20 percent of adults the flap does not seal, however, allowing blood through the hole with coughing or other activities which raise chest pressure. In diving, this can allow blood with microbubbles of inert gas in the venous blood from the body to return directly to the arteries (including arteries to the brain, spinal cord and heart) rather than pass through the lungs, where the bubbles would otherwise be filtered out by the lung capillary system[23]. In the arterial system, bubbles (arterial gas embolism) are far more dangerous because they block circulation and cause infarction (tissue death, due to local loss of blood flow). In the brain, infarction results in stroke, in the spinal cord it may result in paralysis, and in the heart it results in myocardial infarction (heart attack).

Signs and symptomsEdit

Bubbles can form anywhere in the body, but symptomatic sensation is most frequently observed in the shoulders, elbows, knees, and ankles.

This table gives symptoms for the different DCS types. The "bends" (joint pain) accounts for about 60 to 70 percent of all altitude DCS cases, with the shoulder being the most common site. These types are classified medically as DCS I. Neurological symptoms are present in 10 to 15 percent of all DCS cases with headache and visual disturbances the most common. DCS cases with neurological symptoms are generally classified as DCS II. The "chokes" are rare and occur in less than two-percent of all DCS cases. Skin manifestations are present in about 10 to 15 percent of all DCS cases.

Table 1. Signs and symptoms of decompression sickness.
DCS Type Bubble Location Signs & Symptoms (Clinical Manifestations)
BENDS Mostly large joints of the body
(elbows, shoulders, hip,
wrists, knees, ankles)
  • Localized deep pain, ranging from mild (a "niggle") to excruciating. Sometimes a dull ache, but rarely a sharp pain.
  • Active and passive motion of the joint aggravates the pain.
  • The pain may be reduced by bending the joint to find a more comfortable position.
  • If caused by altitude, pain can occur immediately or up to many hours later.
  • Confusion or memory loss
  • Headache
  • Spots in visual field (scotoma), tunnel vision, double vision (diplopia), or blurry vision
  • Unexplained extreme fatigue or behaviour changes
  • Seizures, dizziness, vertigo, nausea, vomiting and unconsciousness may occur, mainly due to labyrinthitis
Spinal Cord
  • Abnormal sensations such as burning, stinging, and tingling around the lower chest and back
  • Symptoms may spread from the feet up and may be accompanied by ascending weakness or paralysis
  • Girdling abdominal or chest pain
Peripheral Nerves
  • Burning deep chest pain (under the sternum)
  • Pain is aggravated by breathing
  • Shortness of breath (dyspnea)
  • Dry constant cough
  • Itching usually around the ears, face, neck, arms, and upper torso
  • Sensation of tiny insects crawling over the skin (formication)
  • Mottled or marbled skin usually around the shoulders, upper chest and abdomen, with itching
  • Swelling of the skin, accompanied by tiny scar-like skin depressions (pitting edema)


Recompression alone was shown to be an effective treatment for minor DCS symptoms by Keays in 1909.[24] Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke[25] and has since become the standard of care for treatment of DCS.[2][26] Recompression is normally carried out in a recompression chamber. In diving, a more risky alternative is in-water recompression.[27][28][29]

Oxygen first aid has been used as an emergency treatment for diving injuries for years.[2] The success of recompression therapy as well as a decrease in the number of recompression treatments required has been shown if first aid oxygen is given within four hours after surfacing.[30] Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators.

Common pressure reductions that cause DCSEdit

The main cause of DCS is a reduction in the pressure surrounding the body. Common ways in which the required reduction in pressure occur are:

  • leaving a high atmospheric pressure environment.
  • ascent through water during a dive. This can happen by rising to the surface at the end of a dive.
  • ascent to altitude in the atmosphere. This can happen by flying in an un-pressurized aircraft.

Leaving a high pressure environmentEdit

The original name for DCS was caisson disease; this term was used in the 19th century, in large engineering excavations below the water table, such as with the piers of bridges and with tunnels, where caissons under pressure were used to keep water from flooding the excavations. Workers who spend time in high-pressure atmospheric pressure conditions are at risk when they return to the lower pressure outside the caisson without slowly reducing the surrounding pressure.

DCS was a major factor during construction of Eads Bridge, when 15 workers died from what was then a mysterious illness, and later during construction of the Brooklyn Bridge, where it incapacitated the project leader Washington Roebling.

Ascent through water during a diveEdit

DCS is best known as an injury that affects underwater divers who breathe gas which is at a higher pressure than surface pressure. The pressure of the surrounding water increases as the diver descends and reduces as the diver ascends. The risk of DCS increases by diving long or deep without slowly ascending and making the decompression stops needed to eliminate the inert gases normally, although the specific risk factors are not well understood. Some divers seem more susceptible than others under identical conditions.

There have been known cases of bends in snorkellers who have made many deep dives in succession. DCS may be the cause of the disease taravana which affects South Pacific island natives who for centuries have dived without equipment for food and pearls.[31]

Two linked factors contribute to divers' DCS, although the complete relationship of causes is not fully understood:

  • deep or long dives: inert gases in breathing gases, such as nitrogen and helium, are absorbed into the tissues of the body in higher concentrations than normal (Henry's Law) when breathed at high pressure.
  • fast ascents: reducing the ambient pressure, as happens during the ascent, causes the absorbed gases to come back out of solution, and form "micro bubbles" in the blood. Those bubbles will safely leave the body through the lungs if the ascent is slow enough that the volume of bubbles does not rise too high.

The physiologist John Haldane studied this problem in the early 20th century, eventually devising the method of staged, gradual decompression, whereby the pressure on the diver is released slowly enough that the nitrogen comes gradually out of solution without leading to DCS.[2][15] Bubbles form after every dive: slow ascent and decompression stops simply reduce the volume and number of the bubbles to a level at which there is no injury to the diver.

Severe cases of decompression sickness can lead to death. Large bubbles of gas impede the flow of oxygen-rich blood to the brain, central nervous system and other vital organs.

Even when the change in pressure causes no immediate symptoms, rapid pressure change can cause permanent bone injury called dysbaric osteonecrosis (DON) "bone cell death from bad pressure".[32] DON can develop from a single exposure to rapid decompression. DON often affects the humerus and femoral heads and can be diagnosed from lesions visible in X-ray images of the bones.[33][34] Unfortunately, X-rays appear normal for at least 3 months after the permanent damage has occurred; it may take 4 years after the damage has occurred for its effects to become visible in the X-ray images. [3]


Decompression tables and dive computers have been developed that help the diver choose depth and duration of decompression stops for a particular dive profile at depth.

Avoiding decompression sickness is not an exact science. Accidents can occur after relatively shallow and short dives. To reduce the risks, divers should avoid long and deep dives and should ascend slowly. Also, dives requiring decompression stops and dives with less than a 16 hour interval since the previous dive increase the risk of DCS. There are many additional risk factors, such as age, obesity, fatigue, use of alcohol, dehydration and a patent foramen ovale. In addition, flying at high altitude less than 24 hours after a dive can be a precipitating factor for decompression illness.

Astronauts aboard the International Space Station preparing for Extra-vehicular activity "camp out" at low atmospheric pressure (approximately 10 psi = 700 mbar) spending 8 sleeping hours in the airlock chamber before their spacewalk. Their spacesuits can operate at 4.7 psi = 330 mbar for maximum flexibility.


Nitrogen is not the only breathing gas that causes DCS. Gas mixtures such as trimix and heliox include helium, which can also be implicated in decompression sickness.

Helium both enters and leaves the body faster than nitrogen, and for dives of three or more hours in duration, the body almost reaches saturation of helium. For such dives the decompression time is shorter than for nitrogen-based breathing gases such as air.

There is some debate as to the decompression effects of helium for shorter duration dives. Most divers do longer decompressions, whereas some groups like the WKPP have been pioneering the use of shorter decompression times by including deep stops.

Decompression time can be significantly shortened by breathing rich nitrox (or pure oxygen in very shallow water) during the decompression phase of the dive. The reason is that the nitrogen outgases at a rate proportional to the difference between the ppN2 (partial pressure of nitrogen) in the diver's body and the ppN2 in the gas that he or she is breathing; but the likelihood of bubbles is proportional to the difference between the ppN2 in the diver's body and the total surrounding air or water pressure.

Ascent to altitude in the atmosphereEdit

People flying in un-pressurized aircraft at high altitude, such as stowaways, or passengers in a cabin that has experienced rapid decompression, or pilots in an open cockpit, can suffer from decompression sickness. Even Lockheed U-2 pilots experienced altitude DCS in the mid-'50s during the Cold War flying over their targets. Divers who dive and then fly in aircraft are at greater risk even in pressurized aircraft because the cabin air pressure is less than the air pressure at sea level. The same applies to divers going into higher elevations by land after diving.

Altitude DCS became a commonly observed problem associated with high-altitude balloon and aircraft flights in the 1930s. In modern-day transport aircraft that fly at high altitudes, cabin pressurization systems ensure that the pressure within the cabin does not fall below the pressure that would be experienced at an altitude of Template:Convert/ftTemplate:Convert/test/A, no matter what the outside air pressure or altitude may actually be during the flight. DCS is very rare in healthy individuals who experience pressures equivalent to this altitude or less. However, since the pressure in the cabin is not actually maintained at sea-level pressure, there is still a small risk of DCS in susceptible individuals (such as recent divers).

There is no specific altitude threshold that can be considered safe for everyone below which it can be assured that no one will develop altitude DCS, but there is very little evidence of altitude DCS occurring among healthy individuals at pressure altitudes below Template:Convert/ftTemplate:Convert/test/A who have not been scuba diving. Individual exposures to pressure altitudes between Template:Convert/ftTemplate:Convert/test/A and Template:Convert/ftTemplate:Convert/test/A have shown a low occurrence of altitude DCS. Most cases of altitude DCS occur among individuals exposed to pressure altitudes of Template:Convert/ftTemplate:Convert/test/A or higher. A US Air Force study of altitude DCS cases reported that only 13 percent occurred below Template:Convert/ftTemplate:Convert/test/A The higher the altitude of exposure, the greater the risk of developing altitude DCS. It is important to clarify that although exposures to incremental altitudes above Template:Convert/ftTemplate:Convert/test/A show an incremental risk of altitude DCS they do not show a direct relationship with the severity of the various types of DCS (see Table 1).

Arterial gas embolism and DCS have very similar treatment because they are both the result of gas bubbles in the body. Their spectra of symptoms also overlap, although those from arterial gas embolism are more severe because they often cause infarction and tissue death as noted above. In a diving context, the two are joined under the general term of decompression illness. Another term, dysbarism, encompasses decompression sickness, arterial gas embolism, and barotrauma.

Ascent to altitude can happen without flying in places such as the Ethiopia and Eritrea highland (8000 feet = about 1.5 miles above sea level) and the Peru and Bolivia altiplano and Tibet (2 to 3 miles above sea level).

Medical treatmentEdit

Mild cases of the "bends" and skin bends (excluding mottled or marbled skin appearance) may disappear during descent from high altitude but still require medical evaluation. If the signs and symptoms persist during descent or reappear at ground level, it is necessary to provide hyperbaric oxygen treatment immediately (100-percent oxygen delivered in a high-pressure chamber). Neurological DCS, the "chokes," and skin bends with mottled or marbled skin lesions (see Table 1) should always be treated with hyperbaric oxygenation. These conditions are very serious and potentially fatal if untreated.

Effects of breathing pure oxygenEdit


One of the most significant breakthroughs in altitude DCS research was oxygen pre-breathing. Breathing pure oxygen before exposure to a low-barometric pressure environment decreases the risk of developing altitude DCS. Oxygen pre-breathing promotes the elimination or washout of nitrogen from body tissues. Pre-breathing pure oxygen for 30 minutes before starting ascent to altitude reduces the risk of altitude DCS for short exposures (10 to 30 minutes only) to altitudes between Template:Convert/ftTemplate:Convert/test/A and Template:Convert/ftTemplate:Convert/test/A. However, oxygen pre-breathing has to be continued without interruption with in-flight, pure oxygen to provide effective protection against altitude DCS.[5][6] Furthermore, it is very important to understand that breathing pure oxygen only during flight (ascent, en route, descent) does not decrease the risk of altitude DCS[5][6], and should not be used instead of oxygen pre-breathing.

Although pure oxygen pre-breathing is an effective method to protect against altitude DCS, it is logistically complicated and expensive for the protection of civil aviation flyers, either commercial or private. Therefore, it is only used now by military flight crews and astronauts for their protection during high altitude and space operations. It is also used by flight test crews involved with certifying aircraft.

Scuba diving before flyingEdit

Divers who ascend to altitudes above sea level increase their risk for developing decompression sickness. Altitude DCS can occur in an airliner, since airliners maintain cabin air pressure corresponding to an altitude of Template:Convert/ftTemplate:Convert/test/A[2][35][36][37] It can happen when moving to high-altitude locations on land after scuba diving—for example, a scuba diver in Eritrea who travels to the country's main airport on the Template:Convert/ftTemplate:Convert/test/A Asmara plateau may be at risk of DCS. It can also happen during cave diving: "Torricellian chambers," found in some caves, are full of air at less than atmospheric pressure, and develop when the water level drops and there is no way for air to get into the chamber.

Diving at altitudeEdit

Diving in water whose surface pressure is below one standard atmosphere (e.g. a high-altitude lake such as Lake Titicaca) may need special high-altitude decompression tables or a specially-programmed dive computer.[2][35][38] (And, on the surface, the divers may suffer effects of altitude hypoxia such as altitude sickness.)

Medical insurance Edit

In the United States, it is common for medical insurance to not cover treatment for the bends that is the result of recreational diving. This is because scuba diving is an elective and "high risk" activity and treatment for decompression sickness is expensive. A typical stay in a recompression chamber will easily cost several thousand dollars, even before emergency transportation is included. Due to this, groups such as Divers Alert Network (DAN) offer medical insurance policies that specifically cover all aspects of treatment for decompression sickness at rates of less than $100 per year.

References Edit

  1. 1.00 1.01 1.02 1.03 1.04 1.05 1.06 1.07 1.08 1.09 1.10 Vann RD (ed). (1989). The Physiological Basis of Decompression. 38th Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 75(Phys)6-1-89.: 437.
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 Brubakk, A. O.; T. S. Neuman (2003). Bennett and Elliott's physiology and medicine of diving, 5th Rev ed., 800, United States: Saunders Ltd..
  3. Benton, B. J. (2001). Acute Decompression Illness (DCI): the Significance of Provocative Dive Profiles.. Undersea Hyperb Med. Abstract 28 (Supplement).
  4. Gerth, W. A., Vann R. D. (1995). Statistical Bubble Dynamics Algorithms for Assessment of Altitude Decompression Sickness Incidence.. US Air Force Technical Report TR-1995-0037.
  5. 5.0 5.1 5.2 5.3 5.4 Pilmanis, A. A. (1990). The Proceedings of the Hypobaric Decompression Sickness Workshop.. US Air Force Technical Report AL-SR-1992-0005.
  6. 6.0 6.1 6.2 6.3 6.4 6.5 6.6 6.7 6.8 6.9 Dehart, R. L.; J. R. Davis (2002). Fundamentals Of Aerospace Medicine: Translating Research Into Clinical Applications, 3rd Rev Ed., 720, United States: Lippincott Williams And Wilkins.
  7. 7.0 7.1 Vann, R. D., W. A. Gerth; P. J. DeNoble; C. F. Pieper; E. D. Thalmann (2004). Experimental trials to assess the risks of decompression sickness in flying after diving.. Undersea Hyperb Med. 31 (4): 431–44.
  8. Elliott, D. H. (1999). Early Decompression experience: Compressed air work.. South Pacific Underwater Medicine Society journal 29 (1).
  9. Vann, R. D., J. R. Torre-Bueno (1984). A theoretical method for selecting space craft and space suit atmospheres.. Aviat Space Environ Med. 55 (12): 1097–102.
  10. Ackles, K. N. (1973). Blood-Bubble Interaction in Decompression Sickness.. Defence R&D Canada (DRDC) Technical Report DCIEM-73-CP-960.
  11. Kindwall, E. P., A. Baz; E. N. Lightfoot; E. H. Lanphier; A. Seireg. (1975). Nitrogen elimination in man during decompression.. Undersea Biomed. Res. 2 (4): 285–97.
  12. Kindwall, E. P. (1975). Measurement of helium elimination from man during decompression breathing air or oxygen.. Undersea Biomed. Res. 2 (4): 277–84.
  13. 13.0 13.1 Francis, T. J. R., D. J. Smith (1991). Describing Decompression Illness.. 42nd Undersea and Hyperbaric Medical Society Workshop. UHMS Publication Number 79(DECO)5-15-91..
  14. McCullough, David (June 2001). The Great Bridge: The Epic Story of the Building of the Brooklyn Bridge, Simon & Schuster.
  15. 15.0 15.1 Boycott, A. E., G. C. C. Damant, John Scott Haldane. (1908). Prevention of compressed air illness. Journal of Hygiene 8: 342–443.
  16. Acott, C. (1999). A brief history of diving and decompression illness.. South Pacific Underwater Medicine Society journal 29 (2).
  17. 17.0 17.1 17.2 17.3 17.4 17.5 17.6 17.7 Fryer, D. I. (1969). Subatmospheric decompression sickness in man., 343, England: Technivision Services.
  18. Karlsson, L., D. Linnarson, M. Gennser, S.L. Blogg, P. Lindholm. (2007). A case of high doppler scores duringaltitude decompression in a subject with a fractured arm.. Undersea Hyperb Med. Abstract 34 (Supplement).
  19. Gerth, W. A., V. L. Ruterbusch, E. T. Long. (2007). The Influence of Thermal Exposure on Diver Susceptibility to Decompression Sickness.. US Naval Experimental Diving Unit Technical Report NEDU-TR-06-07.
  20. Boycott, A. E., J. C. C. Damant. (1908). Experiments on the influence of fatness on susceptibility to caisson disease. J. Hygiene 8: 445–456.
  21. Leigh, B.C., & Dunford, R.G. Alcohol use in scuba divers treated for diving injuries: A comparison of decompression sickness and arterial gas embolism. Alcoholism: Clinical and Experimental Research, 2005, 29 (Suppl.), 157A. Presented at the Annual Meeting of the Research Society on Alcoholism, Santa Barbara, California, June 2005. |url=
  22. Walder, D. N. (1945). The Surface Tension of the Blood Serum in "Bends".. Royal Air Force Technical Report.
  23. Moon, R. E., J. Kisslo (1998). PFO and decompression illness: An update.. South Pacific Underwater Medicine Society journal 28 (3).
  24. Keays, F. J. (1909). Compressed air illness, with a report of 3,692 cases.. Dept Med Publ Cornell Univer Med Coll 2: 1–55.
  25. Yarbrough, O. D., A. R. Behnke (1939). The treatment of compressed air illness using oxygen.. J Ind Hyg Toxicol 21: 213–218.
  26. Berghage, T. E., J. Vorosmarti Jr; E. E. P. Barnard. (1978). Recompression treatment tables used throughout the world by government and industry.. US Naval Medical Research Center Technical Report NMRI-78-16.
  27. Edmonds, C. (1998). Underwater oxygen for treatment of decompression sickness: A review.. South Pacific Underwater Medicine Society journal 25 (3).
  28. Pyle, R. L., D. A. Youngblood. (1995). In-water Recompression as an emergency field treatment of decompression illness.. AquaCorp 11.
  29. Kay, E.; M. P. Spencer. (1999). In water recompression, 108, United States: Undersea and Hyperbaric Medical Society.
  30. Longphre, J. M., P. J. DeNoble; R. E. Moon; R. D. Vann; J. J. Freiberger (2007). First aid normobaric oxygen for the treatment of recreational diving injuries.. Undersea Hyperb Med. 34 (1): 43–49.
  31. Wong, R. M. (1999). Taravana revisited: Decompression illness after breath-hold diving. South Pacific Underwater Medicine Society journal 29 (3).
  32. Ohta Y and Matsunaga H (1974). Bone lesions in divers.. J Bone Joint Surg 56B: 3–15.
  33. Zhang, L. D., J. F. Kang; H. L. Xue. (1990). Distribution of lesions in the head and neck of the humerus and the femur in dysbaric osteonecrosis. Undersea Biomed. Res. 17 (4): 353–358.
  34. British Medical Research Council Decompression Sickness Central Registry and Radiological Panel (1981). Aseptic bone necrosis in commercial divers. A report from the Decompression Sickness Central Registry and Radiological Panel. Lancet 2 (8243): 384–8.
  35. 35.0 35.1 Bassett, B. E. (1982). Decompression Procedures for Flying After Diving, and Diving at Altitudes above Sea Level.. US Air Force School of Aerospace Medicine Technical Report SAM-TR-82-47.
  36. Sheffield, P. J.; R. D. Vann (2002). Flying After Diving Workshop. Proceedings of the DAN 2002 Workshop, 127, United States: Divers Alert Network.
  37. Vann RD, Pollock NW, Freiberger JJ, Natoli MJ, Denoble PJ, Pieper CF (2007). Influence of bottom time on preflight surface intervals before flying after diving. Undersea Hyperb Med 34 (3): 211–20.
  38. Egi, S. M., A. O. Brubakk (1995). Diving at altitude: a review of decompression strategies. Undersea Hyperb Med. 22 (3): 281–300.

See also Edit

External links Edit

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